Oligodendrocytes in the mouse corpus callosum maintain axonal function by delivery of glucose

In the optic nerve, oligodendrocytes maintain axonal function by supplying lactate as an energy substrate. Here, we report that, in acute brain slices of the mouse corpus callosum, exogenous glucose deprivation (EGD) abolished compound action potentials (CAPs), which neither lactate nor pyruvate could prevent. Loading an oligodendrocyte with 20 mM glucose using a patch pipette prevented EGD-mediated CAP reduction in about 70% of experiments. Loading oligodendrocytes with lactate rescued CAPs less efficiently than glucose. In mice lacking connexin 47, oligodendrocyte filling with glucose did not prevent CAP loss, emphasizing the importance of glial networks for axonal energy supply. Compared with the optic nerve, the astrocyte network in the corpus callosum was less dense, and loading astrocytes with glucose did not prevent CAP loss during EGD. We suggest that callosal oligodendrocyte networks provide energy to sustain axonal function predominantly by glucose delivery, and mechanisms of metabolic support vary across different white matter regions

Electromagnetic-induced fission of 238U projectile fragments, a test case for the production of spherical super-heavy nuclei

Isotopic series of 58 neutron-deficient secondary projectiles (205,206At, 205-209Rn, 208-212,217,218Fr, 211-223Ra, 215-226Ac, 221-229Th, 226-231Pa, 231-234U) were produced by projectile fragmentation using a 1 A GeV 238U beam. Cross sections of fission induced by nuclear and electromagnetic interactions in a secondary lead target were measured. They were found to vary smoothly as a function of proton and neutron number of the fissioning system, also for nuclei with large ground-state shell effects near the 126-neutron shell. No stabilization against fission was observed for these nuclei at low excitation energies. Consequences for the expectations on the production cross sections of super-heavy nuclei are discussed.Comment: 20 pages, 13 figure

Complex nuclear-structure phenomena revealed from the nuclide production in fragmentation reactions

Complex structural effects in the nuclide production from the projectile fragmentation of 1 A GeV 238U nuclei in a titanium target are reported. The structure seems to be insensitive to the excitation energy induced in the reaction. This is in contrast to the prominent structural features found in nuclear fission and in transfer reactions, which gradually disappear with increasing excitation energy. Using the statistical model of nuclear reactions, relations to structural effects in nuclear binding and in the nuclear level density are demonstrated.Comment: 19 pages, 14 figures, background information on http://www-w2k.gsi.de/kschmidt

Limits on the production of direct photons in 200 A GeV32^{32}S + Au collisions

A search for the production of direct photons in S+Au collisions at 200\cdotA~GeV has been carried out in the CERN-WA80 experiment. For central collisions the measured photon excess at each p_T, averaged over the range 0.5~GeV/c~ \leq p_T \leq 2.5~GeV/c, corresponded to 5.0\% of the total inclusive photon yield with a statistical error of \sigma_{\rm stat}=0.8\% and a systematic error of \sigma_{\rm syst}=5.8\%. Upper limits on the invariant yield for direct photon production at the 90\%~C.L. are presented. Possible implications for the dynamics of high-energy heavy-ion collisions are discussed

Reactive astrocyte nomenclature, definitions, and future directions

Reactive astrocytes are astrocytes undergoing morphological, molecular, and functional remodeling in response to injury, disease, or infection of the CNS. Although this remodeling was first described over a century ago, uncertainties and controversies remain regarding the contribution of reactive astrocytes to CNS diseases, repair, and aging. It is also unclear whether fixed categories of reactive astrocytes exist and, if so, how to identify them. We point out the shortcomings of binary divisions of reactive astrocytes into good-vs-bad, neurotoxic-vs-neuroprotective or A1-vs-A2. We advocate, instead, that research on reactive astrocytes include assessment of multiple molecular and functional parameters-preferably in vivo-plus multivariate statistics and determination of impact on pathological hallmarks in relevant models. These guidelines may spur the discovery of astrocyte-based biomarkers as well as astrocyte-targeting therapies that abrogate detrimental actions of reactive astrocytes, potentiate their neuro- and glioprotective actions, and restore or augment their homeostatic, modulatory, and defensive functions